The effects of sex and hormonal status on restraint-stress-induced working memory impairment

Shansky, Rebecca M.; Rubinow, Katya B.; Brennan, Avis R.; Arnsten, Amy F.T.

doi:10.1186/1744-9081-2-8

Cited by 95 publications

(55 citation statements)

References 33 publications

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“…For example, rats exposed to either 2 h of restraint stress or administered the pharmacological stressor, FG7142, are impaired on the spatial delayed alternation task, a test of spatial working memory that depends on the medial PFC 19,26 . Performance of this task also requires decision-making capabilities and the ability to inhibit a prepotent but inappropriate response, functions linked to the PFC.…”

Section: Acute Stress Exposure Rapidly Impairs Higher Pfc Functions Imentioning

confidence: 99%

“…However, the addition of inescapable shocks to the restraint paradigm impairs LTP 28 . As restraint stress alone is sufficient to impair the spatial working memory functions of the PFC 26 , it appears that the hippocampus is less sensitive to impairment by acute stress exposure than is the PFC.…”

Section: Acute Stress Exposure Rapidly Impairs Higher Pfc Functions Imentioning

confidence: 99%

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Stress weakens prefrontal networks: molecular insults to higher cognition

2015

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A variety of cognitive disorders are worsened by stress exposure and involve dysfunction of the newly evolved prefrontal cortex (PFC). Exposure to acute, uncontrollable stress increases catecholamine release in PFC, reducing neuronal firing and impairing cognitive abilities. High levels of noradrenergic α1-adrenoceptor and dopaminergic D1 receptor stimulation activate feedforward calcium–protein kinase C and cyclic AMP–protein kinase A signaling, which open potassium channels to weaken synaptic efficacy in spines. In contrast, high levels of catecholamines strengthen the primary sensory cortices, amygdala and striatum, rapidly flipping the brain from reflective to reflexive control of behavior. These mechanisms are exaggerated by chronic stress exposure, where architectural changes lead to persistent loss of PFC function. Understanding these mechanisms has led to the successful translation of prazosin and guanfacine for treating stress-related disorders. Dysregulation of stress signaling pathways by genetic insults likely contributes to PFC deficits in schizophrenia, while age-related insults initiate interacting vicious cycles that increase vulnerability to Alzheimer’s degeneration.

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Section: Acute Stress Exposure Rapidly Impairs Higher Pfc Functions Imentioning

confidence: 99%

Section: Acute Stress Exposure Rapidly Impairs Higher Pfc Functions Imentioning

confidence: 99%

Stress weakens prefrontal networks: molecular insults to higher cognition

2015

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Section: Altered Cognition and Moodmentioning

confidence: 99%

“…For example, restraint-stressed rats display impaired performance in a delayed spatial alternation task, a rodent behavioural test of spatial working memory 91 . The stressed animals made more perseverative errors on the task, suggesting a lack of attention and short-term memory as well as cognitive and/or behavioural inflexibility 91 . Interestingly, correlated neural activity in the PFC and hippocampus is believed to be important for successful performance on this task: hippocampal theta oscillations have been shown to be phase-locked with both theta and single-unit activity in the PFC during the performance of a similar task 92 .…”

Section: Altered Cognition and Moodmentioning

confidence: 99%

Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

et al. 2018

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Post-traumatic stress disorder (PTSD) is a prevalent, debilitating and sometimes deadly consequence of exposure to severe psychological trauma. Although effective treatments exist for some individuals, they are limited. New approaches to intervention, treatment and prevention are therefore much needed. In the past few years, the field has rapidly developed a greater understanding of the dysfunctional brain circuits underlying PTSD, a shift in understanding that has been made possible by technological revolutions that have allowed the observation and perturbation of the macrocircuits and microcircuits thought to underlie PTSD-related symptoms. These advances have allowed us to gain a more translational knowledge of PTSD, have provided further insights into the mechanisms of risk and resilience and offer promising avenues for therapeutic discovery.

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“…In addition, most of the stress-LTP studies have been conducted on male rats. This is an important issue because female rats and women appear to respond differently to acute stress than do the males of each species, a finding which was first suggested by Stratton [36] and then substantiated in contemporary research (Shors [108]; McEwen [109]; Beiko et al [110]; Conrad et al [111]; Kudo et al [112]; Shansky et al [113]; Cahill [114]). Therefore, we acknowledge that our speculation here is based primarily on research conducted on the hippocampus of male rats.…”

Section: Effects Of Stresson Ltp In the Hippocampus Amygdala Andmentioning

confidence: 99%

The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law

et al. 2007

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We have reviewed research on the effects of stress on LTP in the hippocampus, amygdala and prefrontal cortex (PFC) and present new findings which provide insight into how the attention and memory-related functions of these structures are influenced by strong emotionality. We have incorporated the stress-LTP findings into our “temporal dynamics” model, which provides a framework for understanding the neurobiological basis of flashbulb and traumatic memories, as well as stress-induced amnesia. An important feature of the model is the idea that endogenous mechanisms of plasticity in the hippocampus and amygdala are rapidly activated for a relatively short period of time by a strong emotional learning experience. Following this activational period, both structures undergo a state in which the induction of new plasticity is suppressed, which facilitates the memory consolidation process. We further propose that with the onset of strong emotionality, the hippocampus rapidly shifts from a “configural/cognitive map” mode to a “flashbulb memory” mode, which underlies the long-lasting, but fragmented, nature of traumatic memories. Finally, we have speculated on the significance of stress-LTP interactions in the context of the Yerkes-Dodson Law, a well-cited, but misunderstood, century-old principle which states that the relationship between arousal and behavioral performance can be linear or curvilinear, depending on the difficulty of the task.

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The effects of sex and hormonal status on restraint-stress-induced working memory impairment

Cited by 95 publications

References 33 publications

Stress weakens prefrontal networks: molecular insults to higher cognition

Stress weakens prefrontal networks: molecular insults to higher cognition

Brain circuit dysfunction in post-traumatic stress disorder: from mouse to man

The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law

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